Targeted cancer therapies have exploited this “oncogene addiction” concept[6]; this has lead to several successful clinical applications of targeted therapies: BCR-ABL tyrosine kinase inhibition in chronic myeloid leukemia by imatinib[7], inhibition of EGFR in EGFR-mutated non-small cell lung cancers (NSCLC) by erlotinib or gefitinib[8-10], inhibition of BRAF in BRAF-mutated melanoma by vemurafenib[11]and inhibition of ALK in EML4-ALK NSCLC by crizotinib[12]. The gene discussed is BRAF; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.